Fig. 2

PTEN regulates the development of HCC in vitro and in vivo by inhibiting the activation of PI3K/Akt pathway. HHCC cells were transduced with a lentiviral vector encoding full-length human PTEN (oe-PTEN), with those cells infected with a lentiviral vector harboring empty expression vector as controls (vector-NC). a, Representative Western blots of PI3K, Akt, and mTOR proteins and their quantitation in HHCC cells, normalized to GAPDH. b, EdU-stained cells were captured (× 200) to reflect HHCC cell proliferation. c, Representative Western blots of proliferation markers Ki67 and PCNA and their quantitation in HHCC cells, normalized to GAPDH. d, Wound closure was monitored to measure HHCC cell migration (24 h after scratch). e, HHCC cells invading from Matrigel-coated the upper transwell chamber into the lower one. f, Flow cytometric analysis of PI staining was performed to examine the distribution of HHCC cells throughout G0/G1, S, and G2/M phases of the cell cycle. g, Flow cytometric analysis of Annexin V/PI double staining was performed to determine HHCC cell apoptosis. h, Representative HCC xenograft tumors and the growth of HCC xenograft tumor measured every 7 days in nude mice (n = 6). * p < 0.05 compared with vector-NC by unpaired t-test. Data are shown as mean ± standard deviation of three technical replicates